The Rationale of Using Coffee and Melatonin as an Alternative Treatment for Alzheimer’s Disease

Alzheimer’s disease (AD) is a devastating neurodegenerative disease with no current cure. FDA approved drugs have been widely used to address symptoms of AD, but none have been successful in preventing or reversing its effects. As the prevalence of AD increases due to the increased lifespan of the population, it is becoming essential to discover new drugs or find alternative treatment approaches to overcome the potential toxicity induced by current medications. We have noted that coffee and melatonin can play a role in delaying disease onset and improving memory for AD patients. Once these independent discoveries were made, we tested the possibility of using them in combination as therapy for AD. In this review, we are going to summarize the results from various investigations testing caffeine, coffee, and melatonin and present a method for their combined use for maximum treatment efficacy against AD pathogenesis. *Corresponding author: Chuanhai Cao, Department of Pharmaceutical Sciences, College of Pharmacy, University of South Florida, Tampa, FL 33612, USA, Tel: +813-3960742; E-mail: [email protected] Received October 06, 2015; Accepted January 08, 2016; Published January 15, 2016 Citation: Perez A, Li T, Hernandez S, Zhang RY, Cao C (2016) The Rationale of Using Coffee and Melatonin as an Alternative Treatment for Alzheimer’s Disease. J Alzheimers Dis Parkinsonism 6: 205. doi: 10.4172/2161-0460.1000205 Copyright: © 2016 Perez A, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. in coffee, can lower plasma Aβ levels within several hours posttreatment [14]. The ability of caffeine to reduce Aβ levels is attributed to its ability to reduce both betaand gamma-secretase levels in the hippocampus of caffeine-treated Tg mice [13]. This reduction of betaand gamma-secretase levels is of importance because they are responsible for Aβ deposition via the processing of APP. A recent study suggests that caffeine may also exert a protective role through a peripheral mechanism involving red blood cells. In this study, caffeine fully eliminated PKCα activation induced by Aβ through a mechanism involving acetylcholinesterase on the external face of the red blood cell plasma membrane [15]. An additional study investigating the effects caffeine reported a reduction in several proinflammatory and oxidative stress biomarkers typically upregulated in the hippocampus of THYTau22 transgenic mouse model [16]. These significant findings indicate caffeine’s ability to act via the various hypothesized mechanisms of AD pathology. Previous research, has indicated that granulocyte colonystimulating factor (GCSF) has therapeutic effects against cancer [17,18] and neurodegenerative diseases such as AD [19,20] and ALS [21]. Long-term GCSF treatment has been reported to enhance cognitive performance in AD mice through three possible mechanisms: the recruitment of microglia from bone marrow, synaptogenesis, and neurogenesis [22]. Interleukin 10 (IL-10) is an anti-inflammatory cytokine suspected to play a protective function against AD pathogenesis due to the characteristic accompaniment of inflammation with disease progression. Another cytokine, interleukin 6 (IL-6), is presumed Journal of Alzheimer’s Disease & Parkinsonism J o u r n a l o f A lzh eim ers ease & Prkin s o n i s m